The Utility of 18F-fluorodeoxyglucose Positron-Emission Tomography/Computed Tomography in Cutaneous B-Cell Lymphoma.

BACKGROUND: Whole-body integrated positron emission tomography / contrast-enhanced computed tomography (PET/CT) scan is increasingly used in cutaneous lymphomas. However, the value of PET/CT in the detection of cutaneous lesions in primary cutaneous B-cell lymphoma (PCBCL) has barely been investigated. OBJECTIVES: To investigate the diagnostic accuracy of PET/CT in tracking cutaneous involvement in PCBCL. METHODS: A retrospective study was conducted on 35 consecutive patients diagnosed with cutaneous B-cell lymphoma according to the World Health Organization classification who were evaluated with PET/CT as the initial staging procedure before treatment. RESULTS: Thirty-five patients met the study criteria. In two patients extracutaneous disease was detected by PET/CT and CT and confirmed by biopsy. Of the 33 patients with PCBCL, 26 (79%) had small cell PCBCL (18 marginal-zone, 8 follicle-center lymphoma) and 7 (21%) had large cell PCBCL (3 follicle-center, 3 leg-type, 1 indeterminate). PET/CT detected skin lesions in 3 of 26 patients (12%) with small-cell PCBCL as compared to 6 of 7 patients with large-cell PCBLC (86%), a 7.4-fold detection risk (95% confidence interval, 2.4-22, P = 0.004). The PET-positive subgroup was characterized by larger lesion size (P < 0.001) and a higher Ki-67 proliferation index (P < 0.001). CONCLUSIONS: The sensitivity of PET/CT for detecting cutaneous involvement of lymphomas is low for small-cell PCBCL but high for large-cell types, and thus may facilitate therapeutic strategies.

Pigmented demodicidosis - an under-recognized cause of facial hyperpigmentation.

BACKGROUND: There is a paucity of data regarding demodicidosis-associated facial hyperpigmentation. OBJECTIVE: To delineate the clinical, dermoscopic, and histopathologic features of demodicidosis-associated facial hyperpigmentation. METHODS: Clinical and diagnostic data were collected from the medical files of patients who were referred to our outpatient dermatology clinic in 2006-2019 for evaluation of facial hyperpigmentation and were diagnosed with demodicidosis. RESULTS: The cohort included 19 patients (13 male) aged 42-76 years, all with Fitzpatrick skin type 3-4. All presented with mostly asymptomatic dusky, brown-gray, facial pigmentation, localized or diffuse with background erythema in 36.8% of cases, and skin roughness in 26.3%. Dermoscopy yielded characteristic findings of white gelatinous or opaque protrusions from hair follicles or infiltration of follicular openings with an amorphic material. A specific finding was perifollicular and reticulated pigmentation of the affected areas. Findings were confirmed on microscopic (n = 7) and histopathologic (n = 5) studies. Anti-demodectic treatment led to complete (73.6%) or partial (23.4%) resolution of pigmentation within 2 years. CONCLUSION: We describe unique clinicopathological and dermoscopic findings associated with an under-recognized type of facial hyperpigmentation caused by demodex for which we propose the term "pigmented demodicidosis." Demodicidosis should be added to the list of causes of facial hyperpigmentation.

Facial demodicosis in the immunosuppressed state: a retrospective case series from a tertiary referral center.

BACKGROUND: Data on Demodex in the immunosuppressed state is limited, focusing mainly on patients with human immunodeficiency virus and hematological malignancies. The aim of this study was to describe the manifestations of facial demodicosis in diverse immunosuppressive states. METHODS: The medical records of all patients followed at a Demodex outpatient clinic of a tertiary medical center from January 2008 to November 2020 were retrospectively reviewed. Data on patients who were immunosuppressed while with demodicosis were retrieved. RESULTS: The cohort included 28 patients (17 women and 11 men; median age, 58 years). Types of immunosuppression included treatments with hydroxyurea for polycythemia vera/essential thrombocytosis, mycophenolic acid, tacrolimus, and prednisone for liver and/or kidney transplantation, prednisone with cyclosporine/methotrexate/azathioprine/rituximab mainly for autoimmune diseases, mercaptopurine with/without anti-tumor necrosis factor alpha (TNF-α) for Crohn's disease, chemotherapy for neoplasms, anti-TNF-α for psoriasis, and Cushing's syndrome. The clinical types of demodicosis included: papulopustular, erythematotelangiectatic and fulminant rosacea, hyperpigmented, pityriasis folliculorum, pustular folliculitis, and dermatitis. The diverse clinical presentations led to various differential diagnoses. Topical treatment with ivermectin (monotherapy/combination with other treatments) was effective. CONCLUSION: Clinicians treating immunosuppressed patients should be familiar with the different forms of demodicosis and include them in the differential diagnosis of facial eruptions.

[Subacute cutaneous lupus erythematosus induced by terbinafine].

BACKGROUND: The onset of subacute cutaneous lupus erythematosus (SCLE) may be associated with the administration of a variety of drugs. Terbinafine, an oral antifungal agent, which rarely causes cutaneous eruptions, has been implicated as the cause or exacerbation of cutaneous lupus erythematosus in several patients. CASE: A 59-year-old man had received oral terbinafine for onychomycosis. The patient had a history of SCLE, which was in complete remission during the last 5 years. A month after initiating treatment with terbinafine the patient developed SCLE, which was diagnosed clinically and by histology. He had typical papulosquamous lesions. Immunological studies showed elevated titers of anti-nuclear antibodies. Following discontinuation of terbinafine therapy and under the treatment of systemic and topical steroids, a slow resolution of the eruption was noted over several weeks. CONCLUSIONS: This report, along with previous cases described, suggests the association between terbinafine therapy and the onset or exacerbation of SCLE often occurring in a patient with history of systemic lupus erythematosus or SCLE.

Blue-gray mucocutaneous discoloration: a new adverse effect of ezogabine.

IMPORTANCE: Many drugs have been reported to induce skin and/or mucous membrane discoloration. Ezogabine (retigabine) was recently approved as an add-on drug for the treatment of partial seizures in adults with epilepsy. Mucocutaneous discoloration induced by antiepileptic drugs in general and ezogabine in particular has not been previously reported. OBSERVATIONS: Two patients who had received multiple antiepileptic drugs for several years presented with a blue-gray skin dyspigmentation that was most pronounced on the face and lips and was associated with nail pigmentation, blue pigmentation on the hard palate, and black pigment deposits on the conjuctivae. The sole drug common to the therapeutic regimens of both patients was ezogabine. Histopathologically, the main finding was perivascular and periadnexal dermal cells heavily laden with coarse melanin granules, which appeared ultrastructurally as intracellular electron-dense granules. Four months after discontinuing ezogabine, our first patient showed a significant improvement in the mucocutaneous and nail dyspigmentation. CONCLUSIONS AND RELEVANCE: The temporal relationship, clinical features, histologic and ultrastructure findings, and improvement following withdrawal of ezogabine indicate that the dyspigmentation was drug induced. Ezogabine should be added to the list of drugs that can induce mucocutaneous discoloration. The incidence of this significant adverse effect requires further investigation.

Cutaneous B-cell neoplasms mimicking granulomatous rosacea or rhinophyma.

BACKGROUND: Unlike T-cell neoplasms, B-cell lymphoproliferative disorders have a limited clinical spectrum of skin involvement. Cutaneous B-cell neoplasms mimicking rosacea or rhinophyma are rare. OBSERVATIONS: We described 12 patients with B-cell lymphoproliferative neoplasms presenting with a facial eruption clinically mimicking rosacea or rhinophyma. Eleven patients were women; ages ranged from 36 to 81 years. The clinical presentation included small papules on the nose and cheeks and around the eyes mimicking granulomatous rosacea; nodules on the nose, cheeks, chin, or forehead mimicking phymatous rosacea; or a combination of both. Three patients had preexisting erythematotelangiectatic rosacea and 1 had rhinophyma. Based on a clinicopathologic correlation and B-cell clonality analysis, the diagnosis was primary cutaneous follicular center B-cell lymphoma in 4 cases, primary cutaneous marginal zone lymphoma in 6, and skin involvement of chronic lymphocytic leukemia in 2. All patients had an indolent course as expected for their disease. CONCLUSIONS: Cutaneous involvement of B-cell neoplasms may mimic granulomatous rosacea or rhinophyma. This unusual clinical presentation is more common in women and appears in the setting of preexisting rosacea or as a new eruption. Proliferative B-cell disorders should be added to the differential diagnosis of symmetric papular or papulonodular eruptions of the face.

Anetodermic primary cutaneous B-cell lymphoma: a unique clinicopathological presentation of lymphoma possibly associated with antiphospholipid antibodies.

BACKGROUND: Primary cutaneous B-cell lymphoma manifested by anetoderma has been reported in 7 cases. In all, the secondary anetoderma developed in lesions of marginal-zone lymphoma or posttransplant lymphoproliferative disorder resembling marginal-zone lymphoma. The mechanisms underlying the destruction of elastic tissue in anetoderma are unclear. However, there is growing evidence linking primary anetoderma with a wide range of immunologic abnormalities, the most common being the presence of antiphospholipid antibodies. OBSERVATIONS: We analyzed data from 5 patients (3 male, 2 female) with clinical and histopathological features of anetodermic primary cutaneous B-cell lymphoma. Three had marginal-zone lymphoma and 2 had follicle-center cell lymphoma. In all, secondary anetoderma developed in self-regressing nodules/plaques of the lymphoma. Two patients also had lesions clinically and histopathologically compatible with primary anetoderma. Associated immunologic diseases were systemic lupus erythematosus-like disease and rheumatoid arthritis (1 patient each; not in patients with primary anetoderma). Antiphospholipid antibodies were found in 4 patients. CONCLUSIONS: Anetodermic primary cutaneous B-cell lymphoma is a rare and unique clinicopathological manifestation not only of marginal-zone lymphoma, as previously described, but also of follicle-center cell lymphoma. This type of secondary anetoderma, like primary anetoderma, might be associated with immunologic disorders, particularly antiphospholipid antibodies.